Component

Mouse S6 kinase 1 / Rps6kb1

Mouse S6 kinase 1 / Rps6kb1. Species, exposure and limitations are retained in each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. S6K1 depletion blocked insulin-stimulated aspartate-carbon incorporation into RNA and DNA while sparing incorporation of supplied pyrimidines in the compared assays.

    Mouse S6 kinase 1 / Rps6kb1 → Aspartate incorporation into mouse-cell nucleic acids source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse wild-type embryonic fibroblasts; S6K1 siRNA, 15-hour serum starvation, 100 nM insulin for six hours during RNA/DNA labeling, with pyrimidine salvage controls.
    limitations
    An isotope-incorporation endpoint is not a measurement of dietary aspartate efficacy.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Blocking new nucleotide production differs from blocking every route for supplying nucleotides.
    primary_references
    Stimulation of de novo pyrimidine synthesis by growth signaling through mTOR and S6K1. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23429703/ · DOI 10.1126/science.1228792
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 162–168

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse wild-type embryonic fibroblasts; S6K1 siRNA, 15-hour serum starvation, 100 nM insulin for six hours during RNA/DNA labeling, with pyrimidine salvage controls. · source_derived_draft · unverified_draft

    ## l-aspartate-cad-s6k1-flux Blocking new nucleotide production differs from blocking every route for supplying nucleotides. S6K1 depletion blocked insulin-stimulated aspartate-carbon incorporation into RNA and DNA while sparing incorporation of supplied pyrimidines in the compared assays. Model: Mouse wild-type embryonic fibroblasts; S6K1 siRNA, 15-hour serum starvation, 100 nM insulin for six hours during RNA/DNA labeling, with pyrimidine salvage controls. Limitations: An isotope-incorporation endpoint is not a measurement of dietary aspartate efficacy. Evidence access: Primary full text Stimulation of de novo pyrimidine synthesis by growth signaling through mTOR and S6K1. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23429703/ · DOI 10.1126/science.1228792
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Fisetin reduced C/EBP-alpha occupancy at the GLUT4 promoter in mouse 3T3-L1 cells, alongside reduced mTOR/S6K signaling.

    Fisetin → Mouse C/EBP alpha / Cebpa source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Chromatin immunoprecipitation; comparison with rapamycin.
    limitations
    Association and phenocopy do not resolve every direct target.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    A transcriptional step links signaling to glucose transport.
    primary_references
    Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 304–310

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Chromatin immunoprecipitation; comparison with rapamycin. · source_derived_draft · unverified_draft

    ## fisetin-adipocyte-promoter A transcriptional step links signaling to glucose transport. Fisetin reduced C/EBP-alpha occupancy at the GLUT4 promoter in mouse 3T3-L1 cells, alongside reduced mTOR/S6K signaling. Model: Chromatin immunoprecipitation; comparison with rapamycin. Limitations: Association and phenocopy do not resolve every direct target. Evidence access: Primary abstract Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821
    Complete structured claim and evidence

  2. Fisetin reduced p70S6K phosphorylation, increased autophagosome formation and suppressed inflammasome readouts in mouse podocyte models.

    Fisetin → Mouse podocyte NLRP3 inflammasome activation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse podocytes and diabetic kidney study.
    limitations
    Autophagosome number alone does not establish complete autophagic flux.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    Protein recycling and inflammatory signaling changed together.
    primary_references
    Fisetin Attenuates Diabetic Nephropathy-Induced Podocyte Injury by Inhibiting NLRP3 Inflammasome. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35126159/ · DOI 10.3389/fphar.2022.783706

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 400–406

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse podocytes and diabetic kidney study. · source_derived_draft · unverified_draft

    ## fisetin-podocyte-autophagy Protein recycling and inflammatory signaling changed together. Fisetin reduced p70S6K phosphorylation, increased autophagosome formation and suppressed inflammasome readouts in mouse podocyte models. Model: Mouse podocytes and diabetic kidney study. Limitations: Autophagosome number alone does not establish complete autophagic flux. Evidence access: Primary abstract Fisetin Attenuates Diabetic Nephropathy-Induced Podocyte Injury by Inhibiting NLRP3 Inflammasome. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35126159/ · DOI 10.3389/fphar.2022.783706
    Complete structured claim and evidence

  3. Theanine exposure was associated with mTOR pathway activation and phosphorylation of downstream S6 and S6K1 in mice.

    L-Theanine → Mouse mechanistic target of rapamycin / Mtor source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/theanine-research/36615799.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be", "start_char": 0, "end_char": 1077, "text_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be"}
    experimental_model
    Intestinal transporter and phosphorylation assays
    exposure
    Oral L-theanine supplementation in the mouse experiment
    limitations
    Transporter expression and mTOR pathway activation were associated. Without an intervention blocking the proposed pathway, dependency is not established; no human protein-absorption benefit inferred.
    nutrient_topic
    L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
    organism
    Mice
    plain_language
    The signaling pathway and transporter changes occurred together; that alone does not prove the pathway caused every change.
    primary_references
    [theanine-p36615799] L-Theanine Regulates the Abundance of Amino Acid Transporters in Mice Duodenum and Jejunum via the mTOR Signaling Pathway. (2022). https://pubmed.ncbi.nlm.nih.gov/36615799/ DOI: 10.3390/nu15010142
    tissue_or_cell_type
    Intestinal amino acid transport and mTOR signaling

    L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 718–729

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal transporter and phosphorylation assays · source_derived_draft · unverified_draft

    ### theanine-mouse-mtor Theanine exposure was associated with mTOR pathway activation and phosphorylation of downstream S6 and S6K1 in mice. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The signaling pathway and transporter changes occurred together; that alone does not prove the pathway caused every change. organism: Mice tissue_or_cell_type: Intestinal amino acid transport and mTOR signaling experimental_model: Intestinal transporter and phosphorylation assays limitations: Transporter expression and mTOR pathway activation were associated. Without an intervention blocking the proposed pathway, dependency is not established; no human protein-absorption benefit inferred. exposure: Oral L-theanine supplementation in the mouse experiment evidence_span: {"source_cache": "artifacts/theanine-research/36615799.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be", "start_char": 0, "end_char": 1077, "text_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be"} [theanine-p36615799] L-Theanine Regulates the Abundance of Amino Acid Transporters in Mice Duodenum and Jejunum via the mTOR Signaling Pathway. (2022). https://pubmed.ncbi.nlm.nih.gov/36615799/ DOI: 10.3390/nu15010142
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards